In 1988, Hendricks et al. first reported on the presence of carboxypeptidas
e U (U refers to the unstable nature of the enzyme) in human serum. One dec
ade later, the importance of carboxypeptidase U (CPU) in the regulation of
fibrin clot dissolution is well documented. CPU circulates in plasma as an
inactive zymogen, proCPU, that is converted to its active form during coagu
lation and fibrinolysis. CPU cleaves off C-terminal lysine residues exposed
on fibrin partially degraded by the action of plasmin. Because these C-ter
minal lysine residues are important for upregulating the fibrinolytic rate,
CPU thus slows down fibrinolysis.